Five Prime Therapeutics Inc
Q3 2020 Earnings Call Transcript

Published: 3 Nov 2020

[Operator:]

Welcome to the Five Prime Therapeutics Third Quarter 2020 Earnings Call. As a reminder, this conference call is being recorded. I'd now like to introduce your host for today's conference call, Martin Forrest, Vice President, Investor Relations and Corporate Communications. You may begin.

[Martin Forrest:]

Thank you, Sarah. Good afternoon, everyone, and thank you for joining us. The press release for the company's third quarter 2020 financial results was issued earlier today and can be found on our company website. Joining me today are Tom Civik, our President and Chief Executive Officer; Dr. Helen Collins, Chief Medical Officer; and David Smith, our Chief Financial Officer; Andy Rankin, our VP of Research will join us for the Q&A portion of the call today. Today's conference call will include forward-looking statements under the Private Securities Litigation Reform Act of 1995, including statements regarding our research and development programs and financial outlook. Actual results may differ from those indicated by these forward-looking statements due to numerous factors, including those discussed in the Risk Factors section of our SEC filings. Our expectations and assumptions could change. While we may elect to update these forward-looking statements in the future, we specifically disclaim any obligation to do so even if our views change. I'll now turn the call over to Tom.

[Tom Civik:]

Thanks, Martin. Good afternoon everyone and thanks for joining us today for our third quarter 2020 conference call. At Five Prime, we're working to develop new treatment options with large and lasting benefits for people with cancer. Our focus remains on discovering new biological pathways that have the potential to deliver truly novel breakthrough treatments for cancers that require new treatment options. This is hard but important work that we pursue with optimism and courage. I'm proud to say that the Five Prime team has responded well to so many challenges this year with an unwavering focus on advancing our pipeline. I'm also proud to report that because of the team's hard work, our programs remain on track. In my remarks today, I will provide an update on the timing of the top-line data for the FIGHT trial, a brief update on the progress we are making on the 155 program and an introduction to our newest preclinical program 157. Helen will provide updates on our clinical and preclinical program, David will discuss the quarterly financial results and then Andy Rankin, our Head of Research, will join us during Q&A. Starting with bema, I'm pleased to report that we will announce top-line data for the FIGHT trial before the end of the year. As a reminder FIGHT is a global trial with 15 countries represented that is evaluating bema in combination with modified FOLFOX in gastric cancer patients, whose tumors are FGFR2b positive and HER2 negative. This is the first randomized frontline study evaluating FGFR2b positive, HER2 negative gastric tumors. And we are hopeful that the results of the FIGHT trial will reveal a clear path forward for this important potential therapy. Gastric cancer is the third leading cause of cancer deaths globally. And retrospective analyses show that patients with gastric cancer, whose tumors overexpressed FGFR2b, have an even worse prognosis. Unfortunately, the 200,000 global gastric cancer patients, whose tumors overexpressed FGFR2b, have only had chemotherapy to fight their disease. If the FIGHT trial is successful, we believe that we will have a clear path forward to developing a new targeted therapy for frontline FGFR2b positive HER2 negative gastric cancer. We are inspired by this type of challenging work, developing therapies for patients who desperately need new treatment options that leverage our scientific and clinical expertise and allow us to collaborate globally. We look forward to sharing the top-line results for the FIGHT trial with you before the end of the year. Moving on to 155, our CD80-Fc fusion protein, the 155 program remains on track. We've been enrolling patients with warm and hot tumors at the 560 milligram monotherapy dose over the past few months. And we expect to have enough data by year end to inform next steps for this program. This novel first-in-class CD80 fusion protein was developed at Five Prime. And as a result of its two complementary mechanisms of action, direct stimulation of T cells and CTLA-4 checkpoint inhibition, we believe that 155 might have significant potential across many tumor types and lines of therapy. Here is where we are today with the 155 program. For monotherapy, we have completed 11 safety dose cohorts and are at the 560 milligram flat dose. And we are now enrolling additional patients with warm and hot tumors in an exploratory cohort at 560 milligrams where we would expect to see clinical activity. Early in the third quarter, we began enrolling non-small cell lung cancer patients in a dose escalation of 155 in combination with pembrolizumab. We cleared the first dose escalation cohort and are now enrolling patients in the second. We continue to make progress with this important program, and I'm proud to report that the program remains on track. We remain hopeful that this unique science will lead to meaningful patient outcome. Now to our preclinical program. 157 is a novel antibody directed to CCR8, which is a promising immuno oncology target that is expressed by a highly immunosuppressive population at T regulatory cells, specifically within tumors. The 157 antibody is engineered to eliminate these cells and lift the restraints they impose on anti-tumor immunity. Cell line development is underway, 157 is advancing through IND enabling studies and we expect to submit an IND for this program in the first half of 2022. And yesterday, we announced that we will be presenting a poster on 157 at SITC next week. We also continue to advance two other novel research programs and I expect to disclose details about one of these programs in early 2021. I'll end my remarks with an update on cash guidance. We again raised our year-end cash guidance from $80 million to $85 million range to the $100 million to $105 million range. The increase in our cash position will allow us to continue investing in our pipeline. Before turning over the call to Helen and David, I'd like to thank the Five Prime team for the significant progress this year. I joined the team six months ago and I'm very proud to work with this capable and committed team and a very important time for the company. And it gives me great pleasure to share their work and accomplishments with you today. I'll now turn it over to Helen to provide more detail on our clinical and preclinical program. Helen?

[Helen Collins:]

Okay, thank you, Tom. Let's begin with an update on bemarituzumab, or bema as we call it, our FGFR2b monoclonal antibody that's under evaluation, and FGFR2b positive HER2 negative gastric cancer. As Tom mentioned, we expect to report top-line efficacy and safety results from the FIGHT trial before the end of this year. The FIGHT trial is a randomized Phase II double-blind study evaluating the benefits of adding bema to standard modified FOLFOX chemo in frontline FGFR2b positive HER2 negative advanced stage gastric and gastroesophageal cancer. Gastric cancer is a poor prognosis with a median survival in the U.S. of only 10 to 12 months. Frontline chemo hasn't changed in over 10 years, and only provides the progression-free survival of approximately five to seven months. FGF, or fiberglass growth factor, stimulate multiple pathways that are important for cancer cell survival and growth. Bema is a first-in-class antibody that blocks variants of the FGF receptor 2, FGFR2b. In gastric cancer overexpression of FGFR2b on cancer cells is associated with a worst survival. In conducting the Phase II FIGHT trial, over 900 patients were screened in 15 countries and we found approximately 30% of advanced stage HER2 negative gastric cancer in the frontline setting overexpression FGFR2b. This frequency of overexpression was similar across Asia, the U.S. and Europe. Five Prime is the only company with an antibody directed against FGFR2b patients with gastric cancer. Bema's mechanism of action is different than that of the FGFR oral tyrosine kinase inhibitors, which target mutations in genes. It's exciting that the results of this novel approach to treating gastric cancer will be available before the end of the year. And I would like to take a minute to thank the patients, their families, the investigators, the Five Prime team, the Zai Lab, and all our clinical trial partners whose contributions have brought us to this milestone in the bema program. I would now like to turn to FPT155, our first-in-class CD80-Fc fusion protein. FPT155 stimulates the immune system to destroy cancer cells. It does this in two ways by binding directly to CD28 and directly stimulating effector T cell and secondly by binding to CTLA-4, blocking its inhibitory signal and thereby also acting as a checkpoint inhibitor. During the past quarter, we continue to enroll patients with warm and hot tumors at the 560 milligram monotherapy dose. We also completed enrollment of the first cohort in the dose escalation of the combination of FPT155 and pembrolizumab in patients with non-small cell lung cancer. The trial remains on track and we expect to have enough preliminary data by the end of the year to guide our decisions regarding the next steps in this program. Turning to our preclinical program, as Tom announced, we continue to make progress on our three wholly-owned preclinical candidates and we are excited to announce that one of those programs, FPA157, is an anti-CCR8 antibody. FPA157 originated from an in-house bioinformatics screen that sought to identify extracellular targets preferentially expressed by CD4-positive regulatory T cells that reside within the tumor. Our in vivo murine studies confirmed that selective depletion of CCR8 expressing intratumoral Treg cells elicited strong anti-tumor response. 157 offers a unique approach to eliminate a key cellular mediator of immunosuppression in tumors. Our plan is to move through IND enabling studies and into the clinic in the first half of 2022. We will be presenting more details about this program in the poster presentation at SITC next week. As Tom mentioned earlier, there have been no shortage of challenges this year, and I'm proud of Five Prime team which has done an exceptional work to keep our preclinical and clinical programs on track. We're on the cusp of having meaningful and actionable data for our two potentially novel cancer therapies

[David Smith:]

Thanks Helen. Details regarding our financial results can be found in the press release that we issued this afternoon. Turning to our cash position, we finished the quarter with a strong balance sheet. Cash, cash equivalents and marketable securities totaled $112.9 million as of September 30, 2020, compared to $157.9 million as of December 31, 2019. This decrease was primarily attributed to quarterly operating expenses that exceeded quarterly revenues. Collaboration and license revenue for the third quarter of 2020 decreased by $0.9 million, or 31%, to $2 million from $2.9 million for the third quarter of 2019. The decrease was essentially due to a reduction in revenue pursuant to the company's performance obligation under the November 2014 cabiralizumab collaboration with BMS that was partially offset by an increase in collaboration revenue with Zai Lab that resulted from our decision to amend the FIGHT trial from the Phase III to a Phase II design. Research and development expenses for the third quarter of 2020 decreased by $5.5 million or 20% to $21.4 million from $26.9 million for the third quarter of 2019. The decrease was primarily due to lower compensation costs resulting from the October 2019 restructuring, lower clinical trial expense and manufacturing costs along with lower allocated costs, bioanalytics and central lab costs, and a decrease in costs related to preclinical programs. These reductions were partially offset by an impairment charges related to the sublease of a portion of our facility, as well as an increase in companion diagnostics costs related to bema. General and administrative expenses for the third quarter of 2020 increased by $0.5 million, or 4%, to $13.7 million from $13.2 million for the third quarter of 2019. The decrease was primarily due to impairment charges related to the sublease of a portion of our facility and allocated costs that were offset by lower compensation, depreciation, and other miscellaneous and general and administrative costs. Net loss for the third quarter of 2020 was $26.4 million, or $0.74 per basic and diluted share, compared to a net loss of $36.1 million, or $1.03 per basic and diluted share, for the third quarter of 2019. Looking ahead, we expect full-year 2020 net cash used in operating activities to be between $70 and $75 million and estimate ending 2020 with cash, cash equivalents and marketable securities between $100 and $105 million. This represents an increase in our year-end cash guidance that reflects our continued financial discipline, a tax refund under the CARES Act and the use of our ATM. The increase in our cash position will allow us to continue investing in our pipeline and extends our cash runway into 2022. I'd now like to turn the call back over to the operator for the Q&A portion of the call.

[Operator:]

[Operator Instructions] Our first question comes from the line of Etzer Darout with Guggenheim Securities. Your line is now open.

[Etzer Darout:]

Just wanted to know if there's anything we can infer from the timing of the data as far as the pace of PFS events of the drug versus control or maybe how sort of the control arm perform relative to historical data on PFS outcome generally. That's one and then I have a follow up.

[Tom Civik:]

Sure. It's Tom here. Why don't I get started, and then Helen can fill in some gaps. So, just walk back to sort of what we've shared over the last couple quarters, we paused the program back in November of last year with about 150 or exactly 155 patients in the program. And I think as you heard in Helen's comments, progression-free survival for this patient population is just not very good. It averages somewhere between six and seven months. The overall survival is on average a little bit less than a year for the same patient population. And some retrospective analyses, I'll point to the fact that it's probably less than a year for patients whose tumors overexpress FGFR2B. So the data that is available on the FIGHT trial right now is all completely blinded. So we don't have any analysis that's been complete on any of the information yet on the FIGHT trial. So Helen, I don't know if there's anything else you'd like to add to that.

[Helen Collins:]

No, no, I mean, I think, as you've heard us say, we've been guiding the same with the end of this year, beginning of next year and I think we're sort of falling right into the middle of that. So I think things have gone along as we have predicted. And, again, the team has just done a great job despite COVID as they're making sure the data is clean along the way. And so, yes, it's going to be exciting.

[Etzer Darout:]

And then just one quick follow up, I guess, with 155, if you can give us any sense of sort of the number of patients, the different tumor types that we may see on sort of the next update here for the 155 program? Thanks.

[Tom Civik:]

Sure. So, as we announced, we've been enrolling patients with warm and hot tumors at the 560 milligram monotherapy dose. And those warm and hot tumors are the type of tumors that you would expect lung, melanoma, head and neck. And so, we're selecting in those patients right now at the dose that we think we should be seeing clinical efficacy. And then we also announced that we just completed our first dose cohort of the combination trial that is 155 plus pembrolizumab. And that's exclusively lung cancer patients. So we expect that we should have enough patients in hand in-house before the end of the year to inform the next steps on the program.

[Etzer Darout:]

Great, thank you for the updates.

[Tom Civik:]

You're welcome.

[Operator:]

Our next question comes from the line of Jonathan Chang with SVB Leerink. Your line is now open.

[Jonathan Chang:]

First question, at a high level, how should we be thinking about positioning of FPT155 in the treatment landscape relative to YERVOY has used?

[Tom Civik:]

Helen, do you want to get started on this one?

[Helen Collins:]

Yes. I mean, I think, you're right. One of the mechanisms of action is to inhibit CTLA-4. So I think people sometimes make that in comparison to YERVOY, right. I mean, obviously, because this drug also directly stimulates the T cell, it doesn't require the T cell to be activated. So it's going to work on naive as well as already activated T cells. So we think the rationale should be that this will work essentially all - as we have talked about any tumor that's got T cells there, so any warm or hot tumor and the idea would be that we would expect to see better than YERVOY. And I think that's what makes in terms of staying that we think by the end of the year we'll have the data is that by going into the patient population this range of - from non-small cells, [indiscernible] renal cell bladder, head and neck, et cetera, all these patients have been seeing a PD1 prior and except for melanoma, you really would not expect to have any response to YERVOY alone. So I think that that's what's going to allow us to see are we seeing something different or at least do we have a signal of - potentially this is different. Does that help you?

[Tom Civik:]

Yes, and I think maybe just to add to that, I think that's why we're so excited about this potential program is that it really does have broad applicability against many different tumors and multiple different lines of therapy. And as we continue to interrogate the data that we'll [indiscernible] before the end of the year, I think the next steps for the program will be clear.

[Jonathan Chang:]

Second question also on 155, can you provide more granular guidance on when and where investors should expect to see clinical data from the program? Should investors expect to see data by year-end?

[Tom Civik:]

Yes, I think, we've been very intentional in our communication on this topic and just to reiterate it. What we've been saying is that we will have enough information in-house before the end of the year to inform the next steps on the 155 program. We have not yet made a decision on where, what, when and how we'll share that information, but we do believe we'll have enough patients in-house before the end of the year to inform next steps.

[Jonathan Chang:]

And just one last question for me. You've indicated before that you believe 155 is dosing at therapeutically active levels. Can you remind me what the reasons are for that view? Thank you.

[Tom Civik:]

Sure. Helen, do you want to take that one?

[Helen Collins:]

Yes, so it's based on a correlation between our preclinical data where using the expected receptor occupancies, the pharmacokinetics. And then when we went into the clinic, where we started to see a dose dependent increase in the proliferation of T cells at the dose that we would have predicted based on that modeling. And so that's the evidence that we've been saying, okay, this - we should be in a dose range now, where we think that the efficacy is there to be had we will see it. So I would say it's a combination of pharmacokinetics and pharmacodynamics based on modeling from the preclinical to the clinical.

[Operator:]

Our next question comes from the line of Boris Peaker with Cowen. Your line is now open.

[Boris Peaker:]

Right. My first question is just in the COVID environment, I'm just curious if you could comment on the data completeness in the FIGHT trial, specifically, do you have data on if and how many follow-up scans patients may have skipped or delayed due to COVID?

[Tom Civik:]

Yes, maybe let me start with this one and then I'll let Helen add. Then Helen mentioned this in her comments, but I want to reiterate it. This was just extraordinary work that our team did with all the challenges that are going on across the globe. As we mentioned, this is - this 15 different countries we're in the FIGHT trial and then all of them being impacted by COVID in a different way. So the reason we were guiding to such a range of Q4 to Q1 was we wanted to make sure that we could really tighten up and ensure that the data was going to be clean and measurable, so that we could pivot off the information with confidence once we turn over the cards. Helen, I don't know if there's much you can share about the specificity of anything that we've learned about the impact on COVID to the question that was asked.

[Helen Collins:]

No, I mean, I think we've mentioned before back in the spring when I think, of course, maybe COVID is worse now, but at least back then people weren't sure as much how to handle it that we did have some patients who couldn't get into their particular clinic to get a scan, but were able to go elsewhere to get scanned. And again, that was very small number of patients. As we've said we stopped enrolling last November, it is a global trial. And most of the world is not - their medical care has not been impacted as much as maybe once heard in the U.S. And also for cancer patients, this is the front-line gastric cancer. And so patients that are getting treated, they still got into get their treatment and got their scans. And so, we did not have much impact. I shouldn't say zero, but very little. And certainly nothing that in any way makes us think will affect interpretability of the data. We feel very confident about how clean the data is and that includes monitoring.

[Boris Peaker:]

And then my second question is just curious in terms of the bar you're setting for it for the FIGHT trial. What kind of hazard ratio do you think we need to see in this study to justify going into a Phase III trial ultimately?

[Helen Collins:]

We haven't stated exactly - well, go ahead, Tom. Sorry, yes.

[Boris Peaker:]

You go. Helen, this is the challenges of all of us being across the country. Helen, why don't you guys take that one?

[Helen Collins:]

I'm supposed to wait for Tom okay, but I'm an impatient person, and I'm impatient for this data. So, I mean, I think, we're looking to as you know many things have failed in frontline gastric cancer and usually when they fail the hazard ratio, you'll see in the PFS, that someone the point eight range, the few that's been successful have been closer to 4.7. So you know that's the area that we're looking at, right. But we will be looking at response rate and OS, and so now we would expect if this drug is doing what we think, that we will see benefits across the board to all three endpoints, although PFS is optimally.

[Boris Peaker:]

Right.

[Tom Civik:]

Maybe just to add to that, I think it's important to note that this is the first time anyone's done a frontline study in gastric cancer patients that overexpress FGFR2b, and it's a patient population with a really significant made. And the prognosis for these patients is quite bad. So without a new drug being approved, targeted drug in the last 10 years, we feel like it's the FIGHT trials positive, there is a path forward for us to have some really important conversations. And as we advanced the program,

[Operator:]

Our next question comes on of Tony Butler with ROTH Capital. Your line is now open.

[Tony Butler:]

On 155, could you maybe characterize your view of the pace of enrollment? It's kind of a qualified probing question. And has that pace increased or stayed roughly the same? That's point one, if I may. And number two, when you provide that update later this year on the monotherapy will it also include the first dose cohort with the combination, and then I have one follow-up?

[Helen Collins:]

Well, I'll answer your second one first, because I just want to reiterate as well, we have not - we tried to be clear that we will be - may not necessarily be saying something publicly at the end of the year about the 155 data. So what we're saying is that we will have internally enough data that we believe we can say what our next steps are. So I can't promise it, there'll be some public announcements. In terms of enrollment, we've been really quite steady, I mean, that the trial as you may recall is being conducted in Australia and South Korea. So - and in general, again, they've been able to manage, taking care of cancer patients and managing COVID relatively well. So we're on track. I mean, we get anxious to know if suddenly there'll be a week, where maybe nobody will enroll or something. And, but month-by-month, when you look at our average, it's been very steady.

[Tony Butler:]

And last question is on174 anti-CCRA. So there are others, not necessarily marketplace, but certainly that have demonstrated some preclinical data, one from Bristol, as you know, and then one from Janice, that was recently licensed to Gilead. And I'm just curious if I mean, these may have obviously some utility in those IO refractory patients in combination with other agents. But I'm curious if there is anything unique that you could say about your program versus any others to the extent that you have now I'm sure you do have some intelligence on what's going on with the other programs. Thank you.

[Tom Civik:]

Sure, why don't I get started and then I'd love to introduce you to Andy ranking heads up our research team. We're really excited to be announcing 157 our program targeting CCRA. We've been we've been working on this for quite some time. And the team that works with Andy here has done some exceptional work. It's a tricky target. And we had to leverage all of our technical expertise to bring forward this program. And so we were quite excited about the science behind it, but also the complexity of what we were able to build and excited to move it forward very quickly as far as next steps go. So Andy, maybe you can fill in some gaps here.

[Andy Rankin:]

Yes, definitely. Thanks, Yes, Tony, as you know, there are other programs that are out there, targeting CCRA. And I think that speaks volumes to the interest in the excitement around this target. We're aware that there are other programs out, there are similar early stage like ours, and so the kind of information that's available is fairly limited right now. What I can say is that, you know, we're moving full steam ahead. We're really excited about the program and we have a poster that we're going to be presenting at Citi next week. And there'll be additional information about the program there. And we're looking forward to sharing more after that poster presentation as well.

[Operator:]

Our next question comes from the line of Jim Birchenough with Wells Fargo Securities. Your line is now open.

[Q –Nick Abbott:]

It's Nick on for Jim this afternoon. The first question is on bema and maybe you can let us know what you've been doing in the background as we've been waiting for the bema data mature to mature over the last quarter and then if there is a statistically clinically significant increase in PFS, then what should we expect in terms of your detail and timing of next steps and future plans on bema?

[Tom Civik:]

Helen, why don't you take the first one, and then I'll follow up with the second one.

[Helen Collins:]

Well, I mean, I think - I mean, you know, the nice thing about how we designed this study is being double blind, placebo controlled, you know, selected patient population, as you know, we've done all the work with Ventana and PGDx to have really, to have CDs is ready to go, that should this trial read out positively, we will be able to move very quickly, and we've got our trial design down. So I think that kind of answer your question Nick.

[Q –Nick Abbott:]

I mean, I think one of the points you've made is that in all likelihood, you move ahead with a partner, and so manufactured product that would be ready to go into the clinic. I don't know, if you need to extend the shelf life of the product. I mean, just the sort of nuts and bolts of all right, ticking the boxes to make this as attractive as possible to a partner.

[Tom Civik:]

Yes. Hi, Nick, it's Tom here. Yes, I think, as you've heard me say multiple times, we'll be ready to pivot quickly, once we see the data. And we feel really well prepared to advance the program quickly. Helen started to mention it reinforce it. The FIGHT trial was designed and executed up until November of last year as a phase three trial. And we were very confident in the design. Obviously, we've learned a lot about the investigators and the sites across the globe as well. And so we would be leveraging that information quickly. As we think about next steps for the program. You've heard us mentioned many times, there's about 200,000 patients globally, that overexpress FGFR2b in the frontline gastric cancer, and a lot of them are outside the United States. So when we when we get to commercialization of this product, if we're fortunate enough to be there. Clearly, we'll need a partner for that program. In the short-term, after we see the results of the Phase II, and if it's positive, I think we will have options in front of us. And we're fully prepared to explore multiple different options, once we see the data.

[Q –Nick Abbott:]

And then moving to 155. And certainly not last time, maybe you have 155 patients and bema and some program. That's also called 155. So to get something, I think I'm a little puzzled by getting a mechanistic crossover with durably and yet orders of magnitude higher doses, Can you remind us why we should not expect to see excess severe autoimmune events with 155?

[Tom Civik:]

Hi, Helen.

[Helen Collins:]

Yes, so some of it in terms of has to have to answer sort of a mechanistic one that we believe that has to do with the pharmacokinetics. So this has a shorter half-life than your void. And in general, one thinks of inhibitory molecules is requiring certain trough level has to be kept, okay? And whereas for agonism, or activation, it's going to be more the key master the peak level. And so we think that there may be a potential advantage with our drugs, certainly in the preclinical there is that of how this drug is dose was given every three weeks, but that you get this the higher dose, you can get this high peak to stimulate to CD28 and then have the U.S. 560 milligrams, which was maybe somewhere around 8 mcg or kg for - to make sure that you hit the tip of the trough constant throughout the whole three weeks. And state your second question that we're looking at writing down your second question

[Q –Nick Abbott:]

Is really just about how you're avoiding the - wants me to pick up some disk?

[Helen Collins:]

Yes. So we would expect still to get to some extent for I mean, I think anytime you're stimulating T-cells, when you're doing a by inhibiting CTLA-4, or stimulating to CD28, you would expect to get some immune toxicity, right? So I think the question can be whether how the therapeutic window is going to be superior because of this, if you will, sort of intermittent stimulation of the T-cells for CD28. I think you've heard analogy before, it's a little bit like kicking the ball, right? So if you have that how we think of the agonism is that you just give it a quick kick, and then the ball keeps rolling. And then you by using that additional mechanism enlarging that therapeutic window.

[Q –Nick Abbott:]

Okay, thanks. And then for the combo, can you say how many patients were dosed at 70 milligrams and how many you in tentative so 140 milligrams?

[Tom Civik:]

Right now 303 by three, Nick.

[Operator:]

Our next question comes from the line of Eric Joseph with JPMorgan. Your line is now open.

[Eric Joseph:]

Thanks for taking the questions. Just a couple. Well, one clarification on the update with site. Does advancing the program hinge on seeing a static benefit on either PFS or OS? And if not, can you talk a bit about what type of trend do you think would be compelling enough to warrant advancing the program for further in a larger study? And then have a follow up on 155?

[Tom Civik:]

Yes, thanks for the question. I think this gets right back to again the main driver behind us converting this to a Phase II trial. Well, we'll be able to see the results much sooner than we would have before. That's water under the bridge at this point. But the benefit of really being able to interrogate the data before the end of the year, will allow us to determine next steps. And you know, I think we're all really hopeful that it's very clear and for a large patient population. But the benefits here of converting it to a Phase II trial is we'll be able to look for all sorts of different subgroups that they do exist that might inform next steps. Important to note, though, one of the big changes that we made was converting the primary endpoint to PFS, OS is still there, we are still tracking that as well as response rate. And so that will inform where we go with this.

[Eric Joseph:]

Okay, and then 155. And just a follow-up on an earlier question about how 560 was selected as the exploratory dose, was there anything in the way of adverse events that sort of predicted or anticipated to correspond with biologic activity, perhaps GI symptoms based on what we know about the tolerability profile of your way? And do you see any headroom to in terms of safety in order to further those escalate beyond 560 if maybe.

[Tom Civik:]

Helen, do you want to take that one.

[Helen Collins:]

Yes, I mean, as you said before, the dose of 560 has more to do with the PD markers that we've seen in the circulating T-cells that we've seen in patients. And we have not commented on adverse events. We certainly may still consider going to higher doses. And that's - I mean, I'm just trying to Eric just trying to stay within what we said before.

[Operator:]

Thank you. There are no further questions at this time. I would now like to turn the call back to Tom Civik for closing comments.

[Tom Civik:]

All right. Well, thank you. Thanks for all the questions and for joining us today. I'll close today by thanking the Five Prime team for their unwavering focus on our clinical and preclinical programs. Despite this year's challenges. As you heard today, we're on track to report top line data from the FIGHT trial before the end of the year. The 155 program remains on track and we've been enrolling patients with warm and hot tumors at the 560 milligram monotherapy dose over the last few months, we expect that we will have enough data to inform next steps for this program by the end of the year. We introduced 157, a novel antibody directed at CCRA. This is our newest preclinical program and we expect to provide details on another preclinical asset very soon. And finally, we raised our urine cache guidance to 100 to $105 million range. This reflects our continued focus on financial discipline and extends our cash runway into 2022. I'm proud of the work we've done to advance our pipeline. And I'm hopeful that our novel science translates into meaningful patient outcomes in the very near future. So, with that, I just want to say thanks for joining us today and I hope you all stay safe. Take care.

[Operator:]

Ladies and gentlemen, this concludes today's conference call. Thank you for participating. You may now disconnect.